We have recently recognized a morphologic pattern if ischemic myocardial disease characterized by subendocardial vacuolar degeneration, coagulation necrosis without inflammatory cell infiltration, and fibrosis without significant loss of tissue mass. These findings occur in patients with chronic subendocardial ischemia due to severe coronary artery narrowing but without acute coronary thrombosis. In the proposed study we plan to develop a model to evaluate the redistribution of regional myocardial blood flow using the tracer microsphere technique in adult dogs with sudden partial stenosis of the coronary arteries, and in young growing dogs developing chronic progressive coronary occlusion from bands placed on the coronary arteries during early growth. The emphasis will be to develop a model with chronic subendocardial ischemia which is stable during resting conditions. These animals will be subjected to increased myocardial workload situations including exercise and anemia. Regional myocardial blood flow, hemodynamic and electrocardiographic alterations will be monitored during and following such myocardial work overload situations. Hearts will be perfusion fixed with karnovskys fixative for detailed light and electron microscopic study using both qualitative evaluation and quantitative stereologic techniques. Correlations will be made between structural alterations and blood flow changes within the myocardium subjected to both acute and chronic subendocardial ischemia. It is further hypothesized that cardiac hypertrophy may be induced in these animal models with chronic subendocardial ischemia, similar to the development of biventricular hypertrophy found in the majority of patients with severe coronary artery disease resulting in myocardial failure and death. The successful development of this animal model will provide the opportunity to study the pathogenesis as well as modifying factors involved in the lesions of chronic subendocardial ischemia.